Progress and controversy in Alzheimer’s research

The number of people with Alzheimer’s disease is increasing rapidly. Some hail human monoclonal antibodies that clear beta-amyloid deposits from the brain as the first disease-modifying treatments for the condition. However, they are not without controversy — the Food and Drug Administration approved aducanumab despite a lack of evidence for its efficacy and concerns about adverse effects. Medical News Today spoke to a range of experts about the controversy.

According to the World Health Organization (WHO), at least 55 millionTrusted Source people worldwide are currently living with dementia. Dementia most commonly affects those over the age of 65Trusted Source, and with people living longer, the WHO expects the number to reach around 140 million by 2050.

Alzheimer’s disease accounts for 60-70%Trusted Source of dementia cases. A characteristic of Alzheimer’s disease is the presence of beta-amyloid plaquesTrusted Source in the brain, which researchers have hitherto thought to disrupt the transmission of nerve impulses and cause many of the symptoms of Alzheimer’s.

However, the role of beta-amyloid in the disease is still debated.

Medications that clear these plaques were hailed as a great breakthrough in the search for effective Alzheimer’s disease treatments, and several are in development and undergoing clinical trials. But are they the wonder drugs patients, relatives, and researchers are hoping for?

Most Alzheimer’s disease treatments alleviate symptoms and help those with the disease to function for longer than they would without treatment. Two new drugs that have recently received much attention, aducanumab and lecanemab, are human monoclonal antibodiesTrusted Source (hMabs).

These are, according to their manufacturersTrusted Source, the first “disease-modifying” drugs for Alzheimer’s disease.

There are many hMabs under investigation as Alzheimer’s disease treatments. They work by clearing the beta-amyloid plaques that build up in the brain of people with Alzheimer’s. The theory behind them is that since these plaques interfere with the transmission of nerve impulses, clearing the plaques should improve the cognitive abilities of people with Alzheimer’s disease.

However, as yet there is no proof that clearing the beta-amyloid plaques protects individuals from cognitive and functional decline.

Several trials, despite showing a reduction in plaques, have shown little or no difference in symptoms between patients on hMabs and controls on placebo. Some hMabs, such as bapineuzumab, failed after trials demonstrated no clinical efficacy in patients with mild to moderate Alzheimer’s disease. Many others are still going through trials.

MNT